The Real Cause of T2 Diabetes: Fat, Sugar or....
There seems to be this ‘diabetes war’ between fat vs sugar as the “cause” of T2 diabetes, somewhat fueled by the movie What The Health,
Seems to me, the main (but not only) issue is excess calories and excess body fat. Just cutting calories (sometimes dramatically) almost instantly puts diabetes into remission, regardless of the ratio of sugar/carb, fat or protein
1) Here's the data on a new study on the topic. The more weight they lose the more likely they are to be able to put their disease in remission and likely keep it there for a long time provided they keep the weight off:
• Weight gainers: 0% achieved remission (0/76 participants)
• 0-5 kg weight loss (0-11 lbs): 7% (6/89)
• 5-10 kg (11-22 lbs): 34% (19/56)
• 10-15 kg (22-33.1 lbs): 57% (16/28)
• 15+ kg (33.1 lbs): 86% (31/36)
"The program involved an initial 3-month phase of total diet replacement -- 825-853 kcal per day consisting of 59% carbohydrates, 13% fat, 26% protein, and 2% fiber. A food reintroduction period followed for 2 to 8 weeks, which consisted of a diet comprising of 50% carbs, 35% total fat, and 15% protein.
Medpage Article
Weight Management May Reverse T2D
Study participants achieved remission to non-diabetic state
https://www.medpagetoday.com/endocrinol ... etes/69657Lancet Study
Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial
DOI:
http://dx.doi.org/10.1016/S0140-6736(17)33102-1http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)33102-1/fulltext2) In this small pilot study, they reversed diabetes with an 800 calorie diet
Reversal of type 2 diabetes in youth who adhere to a very-low-energy diet: a pilot study.
Diabetologia. 2017 Mar;60(3):406-415. doi: 10.1007/s00125-016-4163-5. Epub 2016 Nov 26.
https://www.ncbi.nlm.nih.gov/pubmed/27889809Abstract
AIMS/HYPOTHESIS:
The aim of the study was to investigate whether a very-low-energy diet (VLED) is a feasible and acceptable treatment option for type 2 diabetes in children and adolescents, and whether adherence can lead to rapid weight loss, reversal of type 2 diabetes and reduced liver fat as seen in adult studies.
METHODS:
Eight participants with type 2 diabetes and obesity, aged 7-16 years, non-medicated (n = 1) or treated with metformin (n = 7) and in some cases insulin (n = 3), followed a VLED (<3360 kJ/day) for 8 weeks, then transitioned to a hypocaloric diet (∼6300 kJ/day) that they followed to 34 weeks. HbA1c, fasting glucose and 2 h post-glucose load plasma glucose (2hG) were determined from fasting blood and an OGTT. Liver fat concentration was quantified using proton magnetic resonance spectroscopy. Adherence was defined as ≥5% weight loss during the 8 week VLED.
RESULTS:
Adherers (n = 5) and non-adherers (n = 3) had median weight loss of 7.5% and 0.5%, respectively, at 8 weeks. Overall, HbA1c (mean [SE] 8.1% [0.7%] to 6.6% [0.5%]; p = 0.004) and 2hG (15.6 [1.6] mmol/l to 11.3 [1.0] mmol/l; p = 0.009) were significantly reduced at 8 weeks compared with baseline. Liver fat was also significantly reduced from baseline (14.7% [2.2%]) to 8 weeks (5.8% [1.7%]; p = 0.001). Only three out of eight participants met non-alcoholic fatty liver disease (NAFLD) criteria (≥5.5%) at 8 weeks, compared with eight out of eight at baseline. The three participants on insulin therapy at baseline were able to cease therapy during the 8 week VLED. At 34 weeks, adherers (n = 5) achieved 12.3% weight loss, none met NAFLD criteria and four did not meet American Diabetes Association criteria for type 2 diabetes.
CONCLUSIONS/INTERPRETATION:
A VLED appears to be a feasible treatment option for some youth with type 2 diabetes on metformin therapy. Youth who agree to participate and adhere to a VLED achieve rapid weight loss, dramatic reductions in liver fat and reversal of type 2 diabetes. This highlights the capacity of a VLED to be used as a first-line treatment option in newly diagnosed youth. A larger trial with a control group and longer follow-up will be required to encourage a change in standard treatment.
3) In this one, they used a 740 calorie diet
Six and 12 Weeks of Caloric Restriction Increases β Cell Function and Lowers Fasting and Postprandial Glucose Concentrations in People with Type 2 Diabetes.
J Nutr. 2015 Sep;145(9):2046-51. doi: 10.3945/jn.115.210617. Epub 2015 Aug 5.
https://www.ncbi.nlm.nih.gov/pmc/articl ... /26246321/Abstract
BACKGROUND:
Caloric restriction alone has been shown to improve insulin action and fasting glucose metabolism; however, the mechanism by which this occurs remains uncertain.
OBJECTIVE:
We sought to quantify the effect of caloric restriction on β cell function and glucose metabolism in people with type 2 diabetes.
METHODS:
Nine subjects (2 men, 7 women) with type 2 diabetes [BMI (in kg/m(2)): 40.6 ± 1.4; age: 58 ± 3 y; glycated hemoglobin: 6.9% ± 0.2%] were studied using a triple-tracer mixed meal after withdrawal of oral diabetes therapy. The oral minimal model was used to measure β cell function. Caloric restriction limited subjects to a pureed diet (<900 kcal/d) for the 12 wk of study. The studies were repeated after 6 and 12 wk of caloric restriction.
RESULTS:
Fasting glucose concentrations decreased significantly from baseline after 6 wk of caloric restriction with no further reduction after a further 6 wk of caloric restriction (9.8 ± 1.3, 5.9 ± 0.2, and 6.2 ± 0.3 mmol/L at baseline and after 6 and 12 wk of caloric restriction, respectively; P = 0.01) because of decreased fasting endogenous glucose production (EGP: 20.4 ± 1.1, 16.2 ± 0.8, and 17.4 ± 1.1 μmol · kg(-1) · min(-1) at baseline and after 6 and 12 wk of caloric restriction, respectively; P = 0.03). These changes were accompanied by an improvement in β cell function measured by the disposition index (189 ± 51, 436 ± 68, and 449 ± 67 10(-14) dL · kg(-1) · min(-2) · pmol(-1) at baseline and after 6 and 12 wk of caloric restriction, respectively; P = 0.01).
CONCLUSIONS:
Six weeks of caloric restriction lowers fasting glucose and EGP with accompanying improvements in β cell function in people with type 2 diabetes. An additional 6 wk of caloric restriction maintained the improvement in glucose metabolism.
4) Here is a study on some ongoing work on reversing diabetes on a 600 calorie diet
Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol
Diabetologia. 2011 Oct; 54(10): 2506–2514.
Published online 2011 Jun 9. doi: 10.1007/s00125-011-2204-7
PMCID: PMC3168743
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3168743/Abstract
Aims/hypothesis
Type 2 diabetes is regarded as inevitably progressive, with irreversible beta cell failure. The hypothesis was tested that both beta cell failure and insulin resistance can be reversed by dietary restriction of energy intake.
Methods
Eleven people with type 2 diabetes (49.5 ± 2.5 years, BMI 33.6 ± 1.2 kg/m2, nine male and two female) were studied before and after 1, 4 and 8 weeks of a 2.5 MJ (600 kcal)/day diet. Basal hepatic glucose output, hepatic and peripheral insulin sensitivity and beta cell function were measured. Pancreas and liver triacylglycerol content was measured using three-point Dixon magnetic resonance imaging. An age-, sex- and weight-matched group of eight non-diabetic participants was studied.
Results
After 1 week of restricted energy intake, fasting plasma glucose normalised in the diabetic group (from 9.2 ± 0.4 to 5.9 ± 0.4 mmol/l; p = 0.003). Insulin suppression of hepatic glucose output improved from 43 ± 4% to 74 ± 5% (p = 0.003 vs baseline; controls 68 ± 5%). Hepatic triacylglycerol content fell from 12.8 ± 2.4% in the diabetic group to 2.9 ± 0.2% by week 8 (p = 0.003). The first-phase insulin response increased during the study period (0.19 ± 0.02 to 0.46 ± 0.07 nmol min−1 m−2; p < 0.001) and approached control values (0.62 ± 0.15 nmol min−1 m−2; p = 0.42). Maximal insulin response became supranormal at 8 weeks (1.37 ± 0.27 vs controls 1.15 ± 0.18 nmol min−1 m−2). Pancreatic triacylglycerol decreased from 8.0 ± 1.6% to 6.2 ± 1.1% (p = 0.03).
Conclusions/interpretation
Normalisation of both beta cell function and hepatic insulin sensitivity in type 2 diabetes was achieved by dietary energy restriction alone. This was associated with decreased pancreatic and liver triacylglycerol stores. The abnormalities underlying type 2 diabetes are reversible by reducing dietary energy intake.
Here is the webpage of the scientific group that is doing this work
http://www.ncl.ac.uk/magres/research/di ... nformationHere is the full text of the write up in Diabetes Care
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3609491/5) I have always found the following study eye-opening in regard to this issue as it really challenges several concepts.
The study compared two diets both containing the same amount of calories (1100), and the same percentages of fat (11%), protein (19%) and carb (71%). The only difference was where the carbs came from. In one group, 43% of the calories came from white sugar. In the other diet, only 4% came from white sugar. Thats 118 grams (around 30 tsps) vs 11 grams (around 3 tsps)
Both groups experienced the same decreases in weight, blood pressure, percentage body fat,and the same changes in total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. There was no difference in the effect of either diet on fasting blood sugar (which went down in both groups)
Why? Total calories were restricted and both groups lost weight. Each group took in around 1100 calories and lost about 7 kgs (almost 15 bs) over the 6 weeks.
Metabolic and behavioral effects of a high-sucrose diet during weight loss
Am J Clin Nutr. 1997 Apr;65(4):908-15.
https://www.ncbi.nlm.nih.gov/pubmed/9094871In response to evidence linking obesity and high amounts of dietary fat, the food industry has developed numerous reduced-fat and nonfat food items. These items frequently derive a relatively large percentage of their energy from sugars and the effect of these sugars on weight regulation is not well known. We studied the comparative effects of high- and low-sucrose, low-fat, hypoenergetic diets on a variety of metabolic and behavioral indexes in a 6-wk weight-loss program. Both diets contained approximately 4606 kJ energy/d with 11% of energy as fat, 19% as protein, and 71% as carbohydrate. The high-sucrose diet contained 43% of the total daily energy intake as sucrose; the low-sucrose diet contained 4% of the total daily energy intake as sucrose. Twenty women aged 40.6 +/- 8.2 y (mean +/- SD) with a body mass index (in kg/m2) of 35.93 +/- 4.8 consumed the high-sucrose diet; 22 women aged 40.3 +/- 7.3 y with a body mass index of 34.93 +/- 4.4 consumed the low-sucrose diet. Mixed-design analysis of variance showed a main effect of time (P < 0.01), with both diet groups showing decreases in weight, blood pressure, resting energy expenditure, percentage body fat, free triiodothyronine (FT3), urinary norepinephrine, and plasma lipids. Small but significant interactions were found between group and time in total cholesterol (P = 0.009) and low-density lipoprotein (LDL) (P = 0.01). Both groups showed decreases in depression, hunger, and negative mood, and increases in vigilance and positive mood with time (P < 0.01). Results showed that a high sucrose content in a hypoenergetic, low-fat diet did not adversely affect weight loss, metabolism, plasma lipids, or emotional affect.
6) From my colleague Jay Kenney, PhD, RDN, Director of Nutrition Research at the Pritikin Longevity Center. (PLC) in a recent discussion on the topic.
".. type 2 DM is driven primarily by excessive calorie intake and excessive body fat stores. Those two factors are far more important than any factors that can play a minor role in the development of insulin resistance and beta-cell failure. We've seen much improved insulin sensitivity for decades at the PLCs when people consume far fewer calories and that happens before they have lost much weight. However, if one stays on a low calorie intake and continues losing more weight you have a win-win situation that allows most type 2 DM patients with sufficient remaining beta-cell function to get off their diabetes meds as insulin resistance is largely reversible with a healthy diet and exercise program provided it reduces calorie intake and leads to long term weight control.
The ratio of FAT/PRO/CHO is far less important. However, at exactly the same calorie intake in weight stable people increasing fat (and especially SFA) at the expense of CHO (perhaps less so fructose rich CHO) seems to slightly increase insulin resistance. Of course, even on the Atkins diet people who lost a lot of weight often got off their diabetes meds so any suggestion that the type of calories one consumes is more important than total calorie intake and change in body fat stores seems rather naïve. Also in weight stable people upping exercise does modestly reduce insulin resistance even though calorie intake does go up to prevent weight loss. Even so some of the effect of exercise may be mediated by increased lean tissue and reduced fat even though body weight stays stable. There is also evidence that a high intake of protein (especially BCAA and specifically valine) can increase insulin resistance in muscle cells directly as the valine is catabolized to HIB. But increased body fat may lead to increased insulin resistance by reducing the ability of insulin to reach muscle cells"
Considering all the above which show that we can easily reverse T2 diabetes in just a week or two using a very low calorie diet regardless of the macronutrient ratios, I think the argument over fat vs sugar as the primary cause of T2 diabetes, is very misguided.
In Health
Jeff